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10.3389/fimmu.2018.01565

http://scihub22266oqcxt.onion/10.3389/fimmu.2018.01565
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C6054963!6054963!30061883
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suck abstract from ncbi


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pmid30061883      Front+Immunol 2018 ; 9 (ä): ä
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  • Type-I Interferons Inhibit Interleukin-10 Signaling and Favor Type 1 Diabetes Development in Nonobese Diabetic Mice #MMPMID30061883
  • Iglesias M; Arun A; Chicco M; Lam B; Talbot CC; Ivanova V; Lee WPA; Brandacher G; Raimondi G
  • Front Immunol 2018[]; 9 (ä): ä PMID30061883show ga
  • Destruction of insulin-producing ?-cells by autoreactive T lymphocytes leads to the development of type 1 diabetes. Type-I interferons (TI-IFN) and interleukin-10 (IL-10) have been connected with the pathophysiology of this disease; however, their interplay in the modulation of diabetogenic T cells remains unknown. We have discovered that TI-IFN cause a selective inhibition of IL-10 signaling in effector and regulatory T cells, altering their responses. This correlates with diabetes development in nonobese diabetic mice, where the inhibition is also spatially localized to T cells of pancreatic and mesenteric lymph nodes. IL-10 signaling inhibition is reversible and can be restored via blockade of TI-IFN/IFN-R interaction, paralleling with the resulting delay in diabetes onset and reduced severity. Overall, we propose a novel molecular link between TI-IFN and IL-10 signaling that helps better understand the complex dynamics of autoimmune diabetes development and reveals new strategies of intervention.
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